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X inactivation and progenitor cancer cells.

Agrelo R - Cancers (Basel) (2011)

Bottom Line: In mammals, silencing of one of the two X chromosomes is necessary to achieve dosage compensation.The 17 kb non-coding RNA called Xist triggers X inactivation.Gene silencing by Xist can only be achieved in certain contexts such as in cells of the early embryo and in certain hematopoietic progenitors where silencing factors are present.

View Article: PubMed Central - PubMed

Affiliation: Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, 1030 Vienna, Austria. agrelo@imp.ac.at.

ABSTRACT
In mammals, silencing of one of the two X chromosomes is necessary to achieve dosage compensation. The 17 kb non-coding RNA called Xist triggers X inactivation. Gene silencing by Xist can only be achieved in certain contexts such as in cells of the early embryo and in certain hematopoietic progenitors where silencing factors are present. Moreover, these epigenetic contexts are maintained in cancer progenitors in which SATB1 has been identified as a factor related to Xist-mediated chromosome silencing.

No MeSH data available.


Related in: MedlinePlus

Epigenetic progenitor context A) Xist can silence the X chromosome in lymphoma cells arrested in a progenitor stage (e.g., double positive cells) and expressing SATB1 (in red). B) Other tumors such as breast cancer cells and cancer cells unresponsive to Xist may reprogram their genome, thus gaining metastatic potential. These malignant progenitors may express SATB1 and may be Xist-responsive.
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f1-cancers-03-02169: Epigenetic progenitor context A) Xist can silence the X chromosome in lymphoma cells arrested in a progenitor stage (e.g., double positive cells) and expressing SATB1 (in red). B) Other tumors such as breast cancer cells and cancer cells unresponsive to Xist may reprogram their genome, thus gaining metastatic potential. These malignant progenitors may express SATB1 and may be Xist-responsive.

Mentions: Lymphoma cells derived from progenitors therefore maintain the epigenetic context that enables the initiation of Xist-mediated gene silencing (Figure 1A). These cells have been suggested to express silencing factors [7]. The special AT-rich binding protein (SATB1) was identified as an initiation factor for Xist-mediated silencing through a comparison of the expression profiles of Xist-responsive and Xist-resistant tumors [7]. Because SATB1 expression was found to be restricted in development, it has been proposed to characterize the cellular context for Xist-mediated silencing in ES cell differentiation and in T lymphocyte development [7].


X inactivation and progenitor cancer cells.

Agrelo R - Cancers (Basel) (2011)

Epigenetic progenitor context A) Xist can silence the X chromosome in lymphoma cells arrested in a progenitor stage (e.g., double positive cells) and expressing SATB1 (in red). B) Other tumors such as breast cancer cells and cancer cells unresponsive to Xist may reprogram their genome, thus gaining metastatic potential. These malignant progenitors may express SATB1 and may be Xist-responsive.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3757410&req=5

f1-cancers-03-02169: Epigenetic progenitor context A) Xist can silence the X chromosome in lymphoma cells arrested in a progenitor stage (e.g., double positive cells) and expressing SATB1 (in red). B) Other tumors such as breast cancer cells and cancer cells unresponsive to Xist may reprogram their genome, thus gaining metastatic potential. These malignant progenitors may express SATB1 and may be Xist-responsive.
Mentions: Lymphoma cells derived from progenitors therefore maintain the epigenetic context that enables the initiation of Xist-mediated gene silencing (Figure 1A). These cells have been suggested to express silencing factors [7]. The special AT-rich binding protein (SATB1) was identified as an initiation factor for Xist-mediated silencing through a comparison of the expression profiles of Xist-responsive and Xist-resistant tumors [7]. Because SATB1 expression was found to be restricted in development, it has been proposed to characterize the cellular context for Xist-mediated silencing in ES cell differentiation and in T lymphocyte development [7].

Bottom Line: In mammals, silencing of one of the two X chromosomes is necessary to achieve dosage compensation.The 17 kb non-coding RNA called Xist triggers X inactivation.Gene silencing by Xist can only be achieved in certain contexts such as in cells of the early embryo and in certain hematopoietic progenitors where silencing factors are present.

View Article: PubMed Central - PubMed

Affiliation: Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, 1030 Vienna, Austria. agrelo@imp.ac.at.

ABSTRACT
In mammals, silencing of one of the two X chromosomes is necessary to achieve dosage compensation. The 17 kb non-coding RNA called Xist triggers X inactivation. Gene silencing by Xist can only be achieved in certain contexts such as in cells of the early embryo and in certain hematopoietic progenitors where silencing factors are present. Moreover, these epigenetic contexts are maintained in cancer progenitors in which SATB1 has been identified as a factor related to Xist-mediated chromosome silencing.

No MeSH data available.


Related in: MedlinePlus